The Role of Prostanoids in the Production of Acute Acalculous Cholecystitis by Platelet-activating Factor

Abstract

Gallbladder tissue from patients with acute acalculous cholecystitis contains increased amounts of prostanoids when compared to normal gallbladder tissue. Platelet-activating factor (PAF) is a potent stimulus of eicosanoid formation. It has been implicated as a mediator of acute inflammatory processes and systemic responses to shock. In this study the role of PAF in acute acalculous cholecystitis was evaluated. Anesthetized cats underwent gallbladder perfusion with a physiologic buffer solution containing [14C]polyethylene glycol as a nonabsorbable tracer to quantitate mucosal water absorption. Platelet-activating factor was infused into the hepatic artery for 2 hours. Control experiments were performed when vehicle alone was infused. Experiments also were performed when indomethacin was administered intravenously and when indomethacin and PAF were administered. Gallbladder mucosal absorption/secretion and perfusate and tissue prostaglandin E (PGE) and 6 keto prostaglandin F1 alpha (6-keto PGF1 alpha) levels were evaluated. Gallbladder inflammation was evaluated by beta-glucuronidase and myeloperoxidase tissue concentrations and by a histologic scoring system. Platelet-activating factor eliminated gallbladder absorption and produced net fluid secretion associated with dose-related increases in perfusate PGE concentrations and gallbladder tissue PGE and 6 keto PGF1 alpha levels when compared to control values. Platelet-activating factor produced significant inflammation in the gallbladder with increases in the histologic score of inflammation and tissue lysosomal enzyme activities. Indomethacin significantly decreased the fluid secretion, prostanoid levels, and inflammation produced by PAF. The results suggest that PAF may induce acute gallbladder inflammation associated with systemic stress through a prostanoid-mediated mechanism.

Contribution of ultrasonography and cholescintigraphy to the diagnosis of acute acalculous cholecystitis in intensive care unit patients

“…The incidence of 4 % in this study is comparable to that in other recent ICU series, which have reported an incidence ranging from 0.5 % to 5 % [3,7,13]. In our study selected patients showed a high incidence of various risk factors described in the literature, namely surgery, trauma [1,15], fasting, total parenteral nutrition [5,17], mechanical ventilation with PEEP [4,16], and narcotics analgesia [6], accounting for 43 % of patients with AAC among the patients suspected.…”

“…Each of these criteria had good sensitivity (90±100 %) but poor specificity (40±60 %) [15]. Combining the three major criteria reduces the sensitivity of US up to 40 % but increases its specificity up to 95 % [15,18]; this was confirmed by our results of 50 % sensitivity and 94 % specificity.…”

“…The test results can be compromised technically by bowel gas, ascites, and abdominal dressings and drains, which explains why pericholecystic fluid and double-layer walls are questionable criteria and were excluded from this study. Nevertheless, some authors regard detection of wall thickening or pericholecystic fluid as more indicative of acute cholecystitis [2,15,19]. The three major criteria chosen in this study have been frequently reported [1,8,18].…”

Acalculous Cholecystitis: Is an Elective Interval Cholecystectomy Necessary

“…Literature 174 also highlights the importance of the humoral response to inflammatory mediator release, splanchnic ischemia and gram-negative bacteria to the pathogenesis of AAC. Lipopolysaccharide elicits a substantial host response by activating coagulation cascades and generating plateletactivating factors, which have been observed in pathogenesis in animal AAC models [23][24][25].…”

Laparoscopic Cholecystectomy for Biliary Tract Emergencies: State of the Art

“…These patients represent a unique challenge, as most are gravely ill from other sources at the time of their initial presentation [35]. Although the pathogenesis of this uncommon syndrome is still unclear, such factors as local ischemia, oxygen radical formation, and inflammatory cytokine release appear to be involved [36]. A number of treatment options are available with the best choice dependent on the clinical status of the patient.…”